Fetal Telencephalon Response
In comparing telencephalon size with the rest of the fetal body (Figure 5), In comparing telencephalon size with the rest of the fetal body (Figure 5), BA fetuses demonstrated a trend of reduced telencephalon size (5%) compared BA fetuses demonstrated a trend of reduced telencephalon size (5%) compared with those of CO (7%) and AA (7%). A similar trend was seen in another with those of CO (7%) and AA (7%). A similar trend was seen in another study [48] that showed improper telencephalon division and development in study [48] that showed improper telencephalon division and development in ethanol induced mouse embryos.
Figure 2. Fetal weights at gestation day 15 across experimental groups N = 254. Figure 2. Fetal weights at gestation day 15 across experimental groups N = 254. Control (CO) saline treated fetuses (N = 117), Binge Alcohol (BA) treated fetuses Control (CO) saline treated fetuses (N = 117), Binge Alcohol (BA) treated fetuses (N = 58), Alcohol-Anthocyanin (AA) treated fetuses (N = 79). Black arrows
(N = 58), Alcohol-Anthocyanin (AA) treated fetuses (N = 79). Black arrows correspond with statistically significant differing values (
correspond with statistically significant differing values (
p p
< 0.05). Values are< 0.05). Values are expressed as means ±standard error.expressed as means ±standard error.
Figure 3. Fetal crown-rump length at gestation day 15 across experimental groups Figure 3. Fetal crown-rump length at gestation day 15 across experimental groups N = 254. Control (CO) saline treated fetuse
N = 254. Control (CO) saline treated fetuses (N = 117), Binge Alcohol (BA) treateds (N = 117), Binge Alcohol (BA) treated fetuses (N = 58), Alcohol-Anthocyanin (AA) treated fetuses (N = 79). Black arrows fetuses (N = 58), Alcohol-Anthocyanin (AA) treated fetuses (N = 79). Black arrows correspond with statistically significant different values (
correspond with statistically significant different values (
p p
< 0.05). Values are< 0.05). Values are expressed as means ± standard error.Figure 4. Representative fetal photograph samples at 15 days gestation from each Figure 4. Representative fetal photograph samples at 15 days gestation from each experimental group demonstrating variations on gross body parameters. 4A: Control experimental group demonstrating variations on gross body parameters. 4A: Control (CO) saline treated mouse fetus; 4B: Binge Alcohol (BA) treated mouse fetus; 4C: (CO) saline treated mouse fetus; 4B: Binge Alcohol (BA) treated mouse fetus; 4C: Alcohol
Alcohol
– –
Anthocyanin (AA) treated mouse fetus.Anthocyanin (AA) treated mouse fetus.Figure 5. Fetus body composition comparing telencephalon size to relative body size, Figure 5. Fetus body composition comparing telencephalon size to relative body size, using a Weibel grid to determine volume density measures. Control (CO) saline treated using a Weibel grid to determine volume density measures. Control (CO) saline treated fetuses (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin fetuses (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin (AA) treated fetuses (N = 11). Values are expressed as means. Circle diameters reflect (AA) treated fetuses (N = 11). Values are expressed as means. Circle diameters reflect relative differences in experimental group body sizes.
relative differences in experimental group body sizes.
The reason behind this pattern can be explained by ethanol
The reason behind this pattern can be explained by ethanol
’s ability to’s ability to
impede the regular migration of pluripotent cells, which plays a vital role in impede the regular migration of pluripotent cells, which plays a vital role in the developing central nervous system [49]. In normal brain development, the the developing central nervous system [49]. In normal brain development, the neural plate acts as a precursor to the developing spinal cord and brain. With neural plate acts as a precursor to the developing spinal cord and brain. With ethanol exposure however, the regular developmental processes in BA fetuses ethanol exposure however, the regular developmental processes in BA fetuses may have been hindered, compromising the integrity of the overall size of the may have been hindered, compromising the integrity of the overall size of the brain [50]. The reducbrain [50]. The reduction in telencetion in telencephalon size is nophalon size is not only due to redut only due to reduced bodyced body size but also reduced telencephalon size relative to body size.
size but also reduced telencephalon size relative to body size.
Figure 6, which details exact measurements of telencephalon area, Figure 6, which details exact measurements of telencephalon area, demonstrates that AA fetuses have relatively similar telencephalon areas demonstrates that AA fetuses have relatively similar telencephalon areas compared with CO fetuses (2.75 versus 3.18 mm
compared with CO fetuses (2.75 versus 3.18 mm22) while BA fetuses (1.47) while BA fetuses (1.47 mm
mm22) have significantly underdeveloped telencephalon areas. The sizeable) have significantly underdeveloped telencephalon areas. The sizeable telencephalon difference between the experimental groups can be attributed to telencephalon difference between the experimental groups can be attributed to
alcohol-induced oxidative stress which is a major mechanism causing cell alcohol-induced oxidative stress which is a major mechanism causing cell death [51]. To explain why telencephalon measurements were similar between death [51]. To explain why telencephalon measurements were similar between AA and CO fetuses, oxidative stress has been shown to decrease upon the AA and CO fetuses, oxidative stress has been shown to decrease upon the administration of cyanidin-3-glucoside, the main anthocyanin compound [52]. administration of cyanidin-3-glucoside, the main anthocyanin compound [52]. Another study supports these protective properties of
Another study supports these protective properties of anthocyaanthocyanins by nins by showingshowing that anthocyanin administration prevented ethanol-induced neuronal cell death that anthocyanin administration prevented ethanol-induced neuronal cell death in rat hippocampal cells [53]. The results from our experiment suggest that the in rat hippocampal cells [53]. The results from our experiment suggest that the ability to maintain the size of the telencephalon in AA fetuses may be ability to maintain the size of the telencephalon in AA fetuses may be attributed to anthocyanin buffering the rate of ethanol-induced neuronal cell attributed to anthocyanin buffering the rate of ethanol-induced neuronal cell death.
death.
Figure 6. Morphometric telencephalon analysis detailing average absolute Figure 6. Morphometric telencephalon analysis detailing average absolute
telencephalon area in each experimental groups. Control (CO) saline treated fetuses telencephalon area in each experimental groups. Control (CO) saline treated fetuses (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin (AA) (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin (AA) treated fetuses (N = 11). Values are expressed as means ± standard errors.
treated fetuses (N = 11). Values are expressed as means ± standard errors.
Figure 7. Fetus body composition comparing liver size to relative body size, using a Figure 7. Fetus body composition comparing liver size to relative body size, using a Weibel grid to determine volume density measures. Control (CO) saline treated fetuses Weibel grid to determine volume density measures. Control (CO) saline treated fetuses (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin (AA) (N = 12), Binge Alcohol (BA) treated fetuses (N = 11), Alcohol-Anthocyanin (AA) treated fetuses (N = 11). Values are expressed as means. Circle diameters reflect treated fetuses (N = 11). Values are expressed as means. Circle diameters reflect relative differences in experimental group body sizes.